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TGM3, a candidate tumor suppressor gene, contributes to human head and neck cancer
BACKGROUND: In our previous study using oligonucleotide microarrays, we revealed that transglutaminase 3 (TGM3) was remarkably down-regulated in head and neck cancer (HNC). However, the potential of TGM3 as a useful biomarker or molecular target for HNC is unclear. METHODS: The transcriptional and p...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4176127/ https://www.ncbi.nlm.nih.gov/pubmed/24289313 http://dx.doi.org/10.1186/1476-4598-12-151 |
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author | Wu, Xiangbing Cao, Wei Wang, Xu Zhang, Jianjun Lv, Zhongjing Qin, Xing Wu, Yadi Chen, Wantao |
author_facet | Wu, Xiangbing Cao, Wei Wang, Xu Zhang, Jianjun Lv, Zhongjing Qin, Xing Wu, Yadi Chen, Wantao |
author_sort | Wu, Xiangbing |
collection | PubMed |
description | BACKGROUND: In our previous study using oligonucleotide microarrays, we revealed that transglutaminase 3 (TGM3) was remarkably down-regulated in head and neck cancer (HNC). However, the potential of TGM3 as a useful biomarker or molecular target for HNC is unclear. METHODS: The transcriptional and post-translational status of TGM3 in HNC cell lines and specimens was detected using real-time PCR and western blot analysis. Bisulfate-treated DNA sequencing was used to analyze the molecular mechanism of TGM3 gene silencing. In addition, the effects of TGM3 on the proliferation, colony formation and induction of apoptosis in vitro and tumorigenicity in vivo were investigated through exogenous expression of TGM3 in HNC cells. Immunohistochemistry was used to evaluate TGM3 expression in large HNC samples. RESULTS: TGM3 was down-regulated in HNC samples and cell lines (P < 0.0001). The hypermethylation of a promoter CpG island was one of the mechanisms of silencing the TGM3 gene in HNC. Exogenous expression of TGM3 in HNC cells could inhibit the proliferation and enhance the apoptosis of HNC cells in vitro and suppress tumor growth in vivo. In addition, TGM3 protein levels were strongly associated with the pathological differentiation of HNC tissues (P = 0.0037). Survival analysis revealed that low TGM3 expression was associated with worse overall survival (P = 0.0002), and TGM3 expression level was an independent predictor in patients with HNC. CONCLUSIONS: The studies prove that TGM3, as a candidate tumor suppressor, contributes to the carcinogenesis and development of HNC and may serve as a useful biomarker for patients with HNC. |
format | Online Article Text |
id | pubmed-4176127 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-41761272014-09-27 TGM3, a candidate tumor suppressor gene, contributes to human head and neck cancer Wu, Xiangbing Cao, Wei Wang, Xu Zhang, Jianjun Lv, Zhongjing Qin, Xing Wu, Yadi Chen, Wantao Mol Cancer Research BACKGROUND: In our previous study using oligonucleotide microarrays, we revealed that transglutaminase 3 (TGM3) was remarkably down-regulated in head and neck cancer (HNC). However, the potential of TGM3 as a useful biomarker or molecular target for HNC is unclear. METHODS: The transcriptional and post-translational status of TGM3 in HNC cell lines and specimens was detected using real-time PCR and western blot analysis. Bisulfate-treated DNA sequencing was used to analyze the molecular mechanism of TGM3 gene silencing. In addition, the effects of TGM3 on the proliferation, colony formation and induction of apoptosis in vitro and tumorigenicity in vivo were investigated through exogenous expression of TGM3 in HNC cells. Immunohistochemistry was used to evaluate TGM3 expression in large HNC samples. RESULTS: TGM3 was down-regulated in HNC samples and cell lines (P < 0.0001). The hypermethylation of a promoter CpG island was one of the mechanisms of silencing the TGM3 gene in HNC. Exogenous expression of TGM3 in HNC cells could inhibit the proliferation and enhance the apoptosis of HNC cells in vitro and suppress tumor growth in vivo. In addition, TGM3 protein levels were strongly associated with the pathological differentiation of HNC tissues (P = 0.0037). Survival analysis revealed that low TGM3 expression was associated with worse overall survival (P = 0.0002), and TGM3 expression level was an independent predictor in patients with HNC. CONCLUSIONS: The studies prove that TGM3, as a candidate tumor suppressor, contributes to the carcinogenesis and development of HNC and may serve as a useful biomarker for patients with HNC. BioMed Central 2013-12-01 /pmc/articles/PMC4176127/ /pubmed/24289313 http://dx.doi.org/10.1186/1476-4598-12-151 Text en Copyright © 2013 Wu et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Wu, Xiangbing Cao, Wei Wang, Xu Zhang, Jianjun Lv, Zhongjing Qin, Xing Wu, Yadi Chen, Wantao TGM3, a candidate tumor suppressor gene, contributes to human head and neck cancer |
title | TGM3, a candidate tumor suppressor gene, contributes to human head and neck cancer |
title_full | TGM3, a candidate tumor suppressor gene, contributes to human head and neck cancer |
title_fullStr | TGM3, a candidate tumor suppressor gene, contributes to human head and neck cancer |
title_full_unstemmed | TGM3, a candidate tumor suppressor gene, contributes to human head and neck cancer |
title_short | TGM3, a candidate tumor suppressor gene, contributes to human head and neck cancer |
title_sort | tgm3, a candidate tumor suppressor gene, contributes to human head and neck cancer |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4176127/ https://www.ncbi.nlm.nih.gov/pubmed/24289313 http://dx.doi.org/10.1186/1476-4598-12-151 |
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